Zobrazeno 1 - 10
of 59
pro vyhledávání: '"Dora B. Krimer"'
Autor:
Jorge Cebrián, María-Luisa Martínez-Robles, Victor Martínez, Pablo Hernández, Dora B. Krimer, Jorge B. Schvartzman, María-José Fernández-Nestosa
Publikováno v:
DNA, Vol 4, Iss 2, Pp 170-179 (2024)
DNA knots are deleterious for living cells if not removed. Several theoretical and simulation approaches address the question of how topoisomerases select the intermolecular passages that preferentially lead to unknotting rather than to the knotting
Externí odkaz:
https://doaj.org/article/7ac973adfbe34014a1daff3d903d6857
Autor:
Jorge Cebrián, Victor Martínez, Pablo Hernández, Dora B. Krimer, María-José Fernández-Nestosa, Jorge B. Schvartzman
Publikováno v:
Biology, Vol 10, Iss 11, p 1195 (2021)
DNA topoisomerases are the enzymes that regulate DNA topology in all living cells. Since the discovery and purification of ω (omega), when the first were topoisomerase identified, the function of many topoisomerases has been examined. However, their
Externí odkaz:
https://doaj.org/article/f86df036de0b4fda942c8af1ffc489bc
Autor:
Vanessa Fernández-Calleja, María-José Fernández-Nestosa, Pablo Hernández, Jorge B. Schvartzman, Dora B. Krimer
Publikováno v:
PeerJ, Vol 7, p e6284 (2019)
Wiskott-Aldrich syndrome (WAS) is a recessive X-linked inmmunodeficiency caused by loss-of-function mutations in the gene encoding the WAS protein (WASp). WASp plays an important role in the polymerization of the actin cytoskeleton in hematopoietic c
Externí odkaz:
https://doaj.org/article/e042f29497994390b7ccea724f19efca
Autor:
Vanessa Fernández-Calleja, Pablo Hernández, Jorge B. Schvartzman, Mario García de Lacoba, Dora B. Krimer
Publikováno v:
PeerJ, Vol 5, p e3432 (2017)
Development of drug resistance limits the effectiveness of anticancer treatments. Understanding the molecular mechanisms triggering this event in tumor cells may lead to improved therapeutic strategies. Here we used RNA-seq to compare the transcripto
Externí odkaz:
https://doaj.org/article/e5bdfcc15a7e4ef0a682e358c2a1e826
Autor:
Christian E. Schaerer, María-José Fernández-Nestosa, Pablo E. Hernández, Jorge Bernardo Schvartzman, Víctor Antonio Vidal Martínez, Dora B. Krimer
Publikováno v:
Digital.CSIC. Repositorio Institucional del CSIC
instname
instname
30 p.-8 fig.
DNA topology changes continuously as replication proceeds. Unwinding of the DNA duplex by helicases is favored by negative supercoiling but it causes the progressive accumulation of positive supercoiling ahead of the fork. This tors
DNA topology changes continuously as replication proceeds. Unwinding of the DNA duplex by helicases is favored by negative supercoiling but it causes the progressive accumulation of positive supercoiling ahead of the fork. This tors
Autor:
María-José Fernández-Nestosa, Víctor Antonio Vidal Martínez, Pablo E. Hernández, Jorge Bernardo Schvartzman, Dora B. Krimer
Publikováno v:
Digital.CSIC. Repositorio Institucional del CSIC
instname
instname
7 p.-4 fig.
The topology of DNA duplexes changes during replication and also after deproteinization in vitro. Here we describe these changes and then discuss for the first time how the distribution of superhelical stress affects the DNA topology
The topology of DNA duplexes changes during replication and also after deproteinization in vitro. Here we describe these changes and then discuss for the first time how the distribution of superhelical stress affects the DNA topology
Autor:
Víctor Antonio Vidal Martínez, Dora B. Krimer, Pablo E. Hernández, Jorge Bernardo Schvartzman, María-José Fernández-Nestosa, Jorge Cebrián
Publikováno v:
E-Prints Complutense. Archivo Institucional de la UCM
instname
Biology, Vol 10, Iss 1195, p 1195 (2021)
Biology
Volume 10
Issue 11
Digital.CSIC. Repositorio Institucional del CSIC
instname
Biology, Vol 10, Iss 1195, p 1195 (2021)
Biology
Volume 10
Issue 11
Digital.CSIC. Repositorio Institucional del CSIC
17p.-5 fig. We dedicate this study to the memory of our friend, mentor, and colleague, Jorge B. Schvartzman.
DNA topoisomerases are the enzymes that regulate DNA topology in all living cells. Since the discovery and purification of ω (omega), w
DNA topoisomerases are the enzymes that regulate DNA topology in all living cells. Since the discovery and purification of ω (omega), w
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::221f394a3dff2e0ab8ac4c80fd084f13
https://eprints.ucm.es/id/eprint/70761/1/biology-10-01195.pdf
https://eprints.ucm.es/id/eprint/70761/1/biology-10-01195.pdf
Publikováno v:
Digital.CSIC. Repositorio Institucional del CSIC
instname
instname
22 p.-5 fig.
During replication, the topology of DNA changes continuously in response to well‐known activities of DNA helicases, polymerases, and topoisomerases. However, replisomes do not always progress at a constant speed and can slow‐dow
During replication, the topology of DNA changes continuously in response to well‐known activities of DNA helicases, polymerases, and topoisomerases. However, replisomes do not always progress at a constant speed and can slow‐dow
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::950a24ef89926355f27a3f8a3441ac40
http://hdl.handle.net/10261/203192
http://hdl.handle.net/10261/203192
Autor:
Dora B. Krimer, Julien Dorier, Andrzej Stasiak, Jorge Bernardo Schvartzman, Pablo E. Hernández
Publikováno v:
Nucleic acids research, vol. 47, no. 14, pp. 7182-7198
Digital.CSIC. Repositorio Institucional del CSIC
instname
Nucleic Acids Research
Digital.CSIC. Repositorio Institucional del CSIC
instname
Nucleic Acids Research
17 p.-10 fig.
Due to helical structure of DNA, massive amounts of positive supercoils are constantly introduced ahead of each replication fork. Positive supercoiling inhibits progression of replication forks but various mechanisms evolved that p
Due to helical structure of DNA, massive amounts of positive supercoils are constantly introduced ahead of each replication fork. Positive supercoiling inhibits progression of replication forks but various mechanisms evolved that p
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d165f9e4e06521e16b7a8a482a42e028
https://serval.unil.ch/resource/serval:BIB_55CCC896580F.P001/REF.pdf
https://serval.unil.ch/resource/serval:BIB_55CCC896580F.P001/REF.pdf
Autor:
María José Fernández-Nestosa, Pablo E. Hernández, Jorge Bernardo Schvartzman, Vanessa Fernández-Calleja, Dora B. Krimer
Publikováno v:
PeerJ
PeerJ, Vol 7, p e6284 (2019)
Digital.CSIC. Repositorio Institucional del CSIC
instname
PeerJ, Vol 7, p e6284 (2019)
Digital.CSIC. Repositorio Institucional del CSIC
instname
18 p.-8 fig.
Wiskott-Aldrich syndrome (WAS) is a recessive X-linked inmmunodeficiency caused by loss-of-function mutations in the gene encoding the WAS protein (WASp). WASp plays an important role in the polymerization of the actin cytoskeleton
Wiskott-Aldrich syndrome (WAS) is a recessive X-linked inmmunodeficiency caused by loss-of-function mutations in the gene encoding the WAS protein (WASp). WASp plays an important role in the polymerization of the actin cytoskeleton